We intend to study the following in normotensive rats (NCR), renovascular hypertensive rats (RHR), and spontaneously hypertensive rats (SHR): microcirculation, regional blood flow, circulating vasoactive agents, and tissue PO2 and K ion. Each of these areas will be quantitated and compared in three circumstances: resting anesthetized state, stressed (hemorrhaged) anesthetized state, and following chemical ablation of the sympathetic nervous system and/or renin-angiotensin system. Television microscopy will be used to observe the cremaster microvasculature in NCR, SHR, and RHR rats. Regional blood flow will be measured by radiolabelled microspheres. Tissue PO2 and K ion will be quantified by microelectrodes. Plasma renin activity will be determined by radioimmunoassay. Plasma catechols will be quantified by high performance liquid chromatography. Experiments are designed to answer the following major questions: (a) Is tissue oxygenation altered by renovascular or spontaneous hypertension?; (b) If so, what is the mechanism responsible for this alteration?; (c) Is tissue hypoxia exaggerated in hypertensive, as compared with normotensive rats in response to stress (hemorphage)?; (d) If so, what is the mechanism responsible for the alteration?; and (e) Is the (presumed) tissue oxygen deficit of hypertension reversible by pharmacological manipulation of the sympathetic nervous system and/or the renin-angiotensin system?